Date: 05 Jun 1997 15:23:25
From: aidsnews@igc.org
Subject: AIDS Treatment News #272
AIDS TREATMENT NEWS Issue #272, June 6, 1997
phone 800/TREAT-1-2, or 415/255-0588
CONTENTS:
Limited Immune Recovery After Treatment with Antiretrovirals,
IL-2; Interview with Clifford Lane, M.D.
Viral Load in Clinical Trials: FDA Advisory Committee Meeting
July 14-15
Meetings Calendar, June 1997 - 1998
***** Limited Immune Recovery After Treatment with
Antiretrovirals, IL-2; Interview with Clifford Lane, M.D.
by John S. James
A person's "CD4 count" (the number of CD4+ T-cells per cubic
millimeter of blood) is used as a rough indicator of immune
system health. But the CD4 cells which are counted are not
all the same. In a healthy individual, there are a billion or
more different kinds of CD4+ T-lymphocytes -- each programmed
to recognize only one specific antigen (foreign substance,
such as part of a protein produced by a bacterium or virus).
In HIV infection, when the CD4 count becomes low (especially
under 200), some of this "repertoire" of cells is lost; it is
probably not immediately restored when the CD4 count rises in
response to antiretroviral treatment (or to treatment with
antiretrovirals plus IL-2 (Proleukin(R)), which causes growth
of the CD4 cells which are still there). Eventually there may
be some natural recovery of the repertoire -- or researchers
might learn how to restore the repertoire by cell
transplantation. Meanwhile, it may be possible for the immune
system to function adequately even though some of its
diversity is lost.
On May 31 AIDS TREATMENT NEWS interviewed Clifford Lane,
M.D., Clinical Director of the U.S. National Institute of
Allergy and Infectious Disease. Dr. Lane is senior
investigator of a research team which published a recent
paper on immune recovery after treatment of HIV with
antiretroviral therapy, or with antiretrovirals plus IL-2.(1)
To introduce the interview, we wrote the following background
section to explain some of the immunology involved.
Background: Different Kinds of CD4+ T-Cells
AIDS TREATMENT NEWS often uses the term "CD4 cells" as a less
complicated way of saying "CD4+ T-lymphocytes" -- which is
technically more accurate, since there are CD4 cells which
are not T-cells at all. This article is only concerned with
T-cells, however.
T-lymphocytes are often named according to the molecules on
their surface. CD4+ T-lymphocytes are those immune-system T-
cells which have the CD4 molecule on their surface; CD8+ T-
lymphocytes have the CD8 molecule. Both cells also have
antigen-specific receptors on their surface. Each cell has
approximately 10,000 or more copies of its antigen-specific
receptor molecules on the cell surface.
The billion or more different kinds of these cells are due to
a billion or more variations in the T-cell receptor. These
variations occur when the cell is formed (usually near the
beginning of life, in the womb or in early childhood). T-
cells begin as undifferentiated stem cells -- special cells
which are able to mature into any kind of blood cell. Certain
stem cells are programmed by the thymus gland to become T-
cells; when this happens, certain genes of the cell combine
randomly, forming the immense number of different possible
combinations. Many of the resulting receptors would cause the
cells to attack the body itself, leading to autoimmune
disease; these unwanted cells are destroyed in the thymus
shortly after they are formed. A billion or more combinations
remain -- probably enough to recognize some parts of all of
the viruses, bacteria, or other disease-causing organisms the
person will ever encounter.
Once a T-cell has been programmed, it can only recognize one
antigen; its receptor cannot change further. It begins as a
"naive" T-cell (one which has never encountered its antigen).
If it does encounter its antigen (many cells never do), it
changes into what is known as a memory cell. In a healthy
adult, about half of the CD4+ T-cells are naive and half are
memory cells; in people with HIV disease, the naive cells are
more rapidly depleted, for reasons which are not entirely
known.
Both naive and memory cells can divide and reproduce in the
blood. This increases the number of cells, which can improve
the immune response. But this kind of cell reproduction
cannot expand the repertoire, because the new cells, whether
naive or memory, are programmed the same as their parent (to
recognize the same antigen). Only new CD4+ T-cells formed in
a thymic environment can add to the repertoire -- and in
adults, the thymus is largely inactive, so these new kinds of
cells are usually formed very slowly.
Any group of cells -- usually just a few cells -- which have
the identical receptor are referred to as a clonal
population, since they probably all arose from a single cell
(or clone). Since there can be a billion or more different
clones in a healthy adult, it is not possible to count and
study them all individually and know which ones are effective
against which diseases. To make it possible to study this
system, the clones have been divided into various families of
related cells; one common system is to divide the many clones
into "V-beta" families (the name is from a region of the
genes which provide a major part of the variability). The
recently published work of Dr. Lane and others(1) studied 22
of these families (which probably account for at least 95% of
the total diversity in this cell population).
In the following interview, we occasionally added explanatory
comments; these are shown [in brackets].
Interview with Clifford Lane, M.D.
ATN: What has been learned about the loss of diversity of
CD4+ T-cells in advanced HIV disease? How much of the
immunity comes back when the total CD4 count increases after
treatment with antiretrovirals, or with IL-2 in addition to
antiretrovirals?
Dr. Lane: The ability of the immune system to come back,
following antiretroviral therapy, will depend on how much has
been destroyed. The reason for this limited recovery is that
the immune system is initially generated by stem cell
differentiation through a thymic environment -- and this
particular pathway [involving the thymus] appears to play a
very small role in the mature adult human.
This has been confusing to immunologists because much of the
work on this aspect of immunology has been done with mice and
rats -- in which the lifespan of the animal and the lifespan
of the thymus are not that different. But in humans, thymic
function drops off greatly in childhood and then drops again
in puberty, and the adult has very little remaining. There is
some left; how much varies between people.
To understand this, it helps to look first at what happens to
the adult human immune system following a major insult when
HIV is not there -- for example, when the system is decreased
through radiation or chemotherapy. The immune system can come
back, but generally not all the way back to where it was.
With HIV, it is now clear that as immune health declines, the
diversity in the repertoire of cells declines. You can block
the virus and allow the total count to come up -- but what
comes up, at least immediately, is mainly an expansion of the
cells that were already there. The number of cells can
increase to a new plateau, which may be higher or lower
depending on the patient, and depending on the level of
ongoing viral replication.
Even though the count does not go all the way back to normal,
and some of the original diversity of cells is missing, you
might still have an adequately functioning immune system.
This is because the immune system has great redundancy in it.
If the virus can be stopped, then with repeated antigenic
challenge, what had been in effect a second-line set of
clones can expand and become a first-line defense. The T-cell
immune system's ability to adapt to the environment is
phenomenal; this adaptability is its key characteristic.
Animal studies suggest that the number of different T-cell
receptors you need [to maintain good health] is much smaller
than the number you can make. You do not necessarily need a
great number to be protected. In studies in rats, in which
cells were transferred from a healthy animal to an ablated
animal [one with its immune system destroyed], it was found
that the best protection was from the memory cells compared
to the naive cells -- and that it only takes a transfer of
about a thousand clones to provide a good defense [in the
animal; no similar experiment could ethically be done with
humans]. The immune system can adapt, and low-affinity clones
[those which are not especially good in recognizing a
disease-causing organism] can expand to meet the needs of the
environment.
ATN: And in HIV disease, the loss of diversity begins even at
CD4 counts above 200, but becomes worse below 200?
Dr. Lane: It appears to be more pronounced as the count drops
below 200.
ATN: Is there a similar repertoire with CD8 cells as with CD4
cells?
Dr. Lane: The CD4 repertoire is quite similar over time for a
person, almost like a fingerprint; we can look at a diagram
of the repertoire even after a year or more, and often tell
whose blood it is. The patterns do change if a person has HIV
infection, but the changes tend to be gradual over time. CD8
T-cells, on the other hand, are always coming and going in
the blood, and they have a very chaotic repertoire. This
difference may reflect the role of the CD4 cells as the
control center of the immune system, vs. some of the more
effector limbs of the system [such as the CD8 cells], that
need to change more rapidly to deal with whatever the
emergency is. The CD4 cells are more for surveillance,
keeping an eye on things.
ATN: I heard that in cancer, after chemotherapy there could
be some slow immune recovery over years.
Dr. Lane: That is true, but usually the system does not get
all the way back to normal. Part of this slow recovery over
time may be a trickling of cells through a thymic
environment, in patients who have some remaining degree of
thymic function.
ATN: What does this mean for prophylaxis of opportunistic
infections -- pneumocystis, for example?
Dr. Lane: To me the first message is that if you are
following a patient with a CD4 count of 50 who is on Bactrim,
and start combination antiretroviral treatment and a month
later the count is over 200, I would not stop prophylaxis at
that point, as [immune recovery] takes time. Six months out,
it would be a good question for a clinical trial. We simply
do not know the answer today. Each physician needs to use his
or her own judgment about the risks and benefits of
prophylaxis [when it might or might not still be necessary,
after partial immune recovery due to antiretroviral
treatment]. The risk of an opportunistic infection is
probably somewhat less [after the T-cell count rise] -- but
how much less is unclear. It's not black and white; the
immune system is not static but is actively changing, to try
to do its best in host defense. Once the negative influence
of HIV is taken away, what is left of the immune system can
probably do a pretty good job.
IL-2 and CD4 Cell Increase
[Note: Dr. Lane suggested that AIDS TREATMENT NEWS disclose
that, as part of his government duties, he received a patent
for his work with IL-2.]
ATN: In the recent paper(1), your team studied not only
antiretroviral therapies to increase T-cell counts, but also
IL-2 [which stimulates the growth of T-cells]. Is it the same
picture with IL-2, of increasing only the cells that are
already there?
Dr. Lane: Yes, with IL-2, the cell increases you get are an
expansion of the cells already present. But there is one
slight difference. The paper(1) looks at the increase in two
different ways. Besides the V-beta families, our study also
measured naive vs. memory cells, and found that in the
setting of antiretroviral therapy alone they increased in
parallel. (Naive cells are depleted most rapidly in HIV, and
some patients with CD4 counts under 50 may have almost no
naive cells.)
With IL-2 there is some preferential increase in naive cells.
But though this makes the ratio of naive to memory cells more
normal, it is probably not a benefit -- it may make the
increase with IL-2 a little less desirable than the increase
with antiretrovirals. Because with antiretrovirals, the cells
that increase will tend to be in proportion to what antigens,
what pathogens, are there. So, with antivirals alone, you may
get a cell expansion which is directed more appropriately to
each individual patient -- while with IL-2 you may get more
of an expansion of whatever clones are there.
I do believe that the new cells [produced by IL-2 treatment]
are totally functional CD4 T-cells.
ATN: But the only way to prove that is a large clinical trial
-- since we do not have an accepted marker, like viral load,
for immune treatments?
Dr. Lane: I feel very strongly that a phase III trial is
needed. Before using IL-2 on a large scale for HIV treatment,
we need to be sure that its benefits outweigh its
disadvantages. There is often a burst of virus when IL-2
stimulates T-cell growth. And there are side effects of this
drug. The T-cell increases are substantial and impressive.
But unless they provide clinical benefit, they would not be
very meaningful.
The problem is that to deliver IL-2 easily, you want to work
with an earlier patient population -- because then you can
use lower doses and give the drug less often. But to obtain
clinical endpoints in an early cohort requires many patients
to be followed for a long time.
This is a central challenge now in HIV medicine -- how do we
determine the best way to manage patients? While short
studies looking at changes in viral load will be helpful in
determining the most potent antiviral drugs, I am not sure
they will give us a clear picture on how best to manage
patients over years.
ATN: What patient population should be studied with IL-2?
Dr. Lane: We are talking about those with a CD4 count of 350
and above -- and letting the antiretroviral strategy be at
the discretion of the physician-investigator.
ATN: In that case, if the antiretrovirals work well enough,
the trial will not get clinical endpoints, and it will not
prove anything. But in case the antivirals do not work well
enough over the long period, then you will see if there is
any additional benefit from the IL-2. Is that the rationale
of this trial?
Dr. Lane: Exactly. You are trying to increase your margin,
increase the safety net. If drug resistance eventually
develops, the patient will probably be better off with a CD4
count of perhaps 1,000 than with a CD4 count of 200. But if
we can totally block the virus and maintain a healthy immune
system with antiretrovirals alone, there will be no role for
IL-2.
We now know how to use IL-2 with less toxicity than before
and how to generate similar results with self-administered
subcutaneous dosing(2), especially in early patients (in
advanced patients you need higher doses). In early patients,
my guess is that after three 5-day cycles of IL-2 over a six
month period of time, we will be able to almost double the
CD4 count. Then we can spread out the cycles of IL-2 -- maybe
once a year, or once every two years.
ATN: Measure the CD4 count and give IL-2 only when they need
it?
Dr. Lane: Yes. This is like the induction vs. maintenance
used with many different kinds of therapies.
ATN: But with advanced patients you would have to treat more
often?
Dr. Lane: Probably. It would become a more difficult clinical
trial to carry out. And the answer for one group of patients
should apply to the other as well -- since the key question
is whether increasing the CD4 count as a result of IL-2
therapy is of clinical benefit. I think that the strategy of
running a trial with more patients for a longer period of
time, but with a regimen which is easier to administer, is
probably more effective [than a smaller trial which uses a
higher dose of IL-2 with more side effects].
ATN: The ethics and acceptability of this trial look quite
good. It would not interfere with peoples' antiretroviral
treatment at all; they would use whatever they want, and the
IL-2 treatment would not be onerous.
Dr. Lane: This trial would find out if the benefit of T-cell
expansion with IL-2 is enough to warrant the cost and
trouble, and the side effects.
ATN: Is such a trial likely?
Dr. Lane: I believe we are going to do it -- but am not yet
entirely sure of all the researchers and organizations who
will be there when we start. A group of European and U.S.
investigators who have expressed strong interest in such a
trial will be at a meeting in mid June to make some final
decisions on a draft protocol for review by the entire group.
Hopefully at a meeting of the CPCRA (NIAID's Community
Program for Clinical Research on AIDS) in July, we will come
to final decisions on the protocol. In addition to the CPCRA
and intramural NIAID, a consortium of European and Australian
investigators, and the Canadian trials network, are currently
part of this effort. My hope is that we will build the
support close to a critical mass, and then get the additional
help that we need so that this trial can happen.
The data are quite solid. The clinical data we have fit with
the immunologic data. The viral levels certainly have not
been going up in the randomized study. Our knowledge of many
of the immunological and virological subtleties is in place
as well.
[Note: An earlier clinical trial in 60 patients(3) found that
when IL-2 was added to an antiretroviral regimen for 12
months, the average CD4 count increased from 428 to 916. In
the control group with the same treatment except for the IL-
2, the average CD4 count fell from 406 to 349. But this trial
was too small to show whether or not increasing the CD4 count
in this way was beneficial to patients. In the long-term
followup of this cohort there have been seven patients with
AIDS-defining events among the patients originally randomized
to the control arm, compared to two AIDS-defining events
among the patients originally randomized to IL-2.]
References
1. Connors M, Kovacs JA, Krevat S, Gea-Banacloche JC, Sneller
MC, Flanigan M, Metcalf JA, Walker RE, Falloon J, Baseler M,
Stevens R, Feuerstein I, Masur H, and Lane HC. HIV Infection
induces changes in CD4+ T-cell phenotype and depletions
within the CD4+ T-cell repertoire that are not immediately
restored by antiviral or immune-based therapies. NATURE
MEDICINE May 1997; volume 3, number 5, pages 533-540.
2. Davey, Jr., RT, Chaitt DG, Piscitelli SC and others.
Subcutaneous administration of interleukin-2 in HIV-1
infected individuals. JOURNAL OF INFECTIOUS DISEASES 1997;
volume 175, number 4, pages 781-789.
3. Kovacs JA, Vogel S, Albert JM, and others. Controlled
trial of interleukin-2 infusions in patients infected with
the human immunodeficiency virus. NEW ENGLAND JOURNAL OF
MEDICINE October 31 1996; volume 335, number 18, pages 1350-
1356.
***** Viral Load in Clinical Trials: FDA Advisory Committee
Meeting July 14-15
An important public meeting on using sustained changes in
viral load as a substitute for clinical endpoints in certain
trials of antiretroviral drugs will be held July 14 and 15
near Washington, D.C. The FDA's Antiviral Drugs Advisory
Committee will meet from 8:30 a.m. to 5:00 p.m. each day in
Room 204 of the Armory Place, 925 Wayne Avenue, Silver
Spring, Maryland. (On July 16 the Advisory Committee will
also meet at the same time and place, but on a separate topic
-- approval of AmBisome(R) liposomal amphotericin B as
empirical therapy for presumed fungal infection in febrile,
neutropenic patients.) All three days of meetings are open to
the public.
Persons who want "to participate in the open public hearing
or to submit data, information or views to the committee" may
do so during a public hearing scheduled for July 14 from 11
a.m. to noon. Those who want to speak should notify Rhonda
Stover or John Schupp, at the Center for Drug Evaluation and
Research (HFD-21), Food and Drug Administration, 301/443-
5455, or by fax at 301/443-0699, by July 7.
The Armory Place is near the Silver Spring Metro stop. Long-
term metered parking is available at Fenton Street and
Pershing Drive (payable with quarters only), and there is
other parking in the area.
If there are any changes to the meeting schedule, they will
be announced on the FDA Advisory Committee Hotline, 800/741-
8138 or 301/443-0572. The 5-digit code number for information
about the Antiviral Drugs Advisory Committee is 12531.
***** Meetings Calendar, June 1997 - 1998
The following list includes research conferences (where new
scientific information will be presented), plus selected
other meetings that may interest our readers. We have not
included invitation-only conferences.
If you know of other meetings that should be on this list,
please let us know.
June 1997
** New Perspectives in Treatment: Eradication, Suppression, &
Lifelong Adherence: Where Are We? June 14, Cambridge,
Massachusetts. Contact: New England AIDS Education and
Training Center, 617/566-2283.
** HIV Treatment in the New Millennium: Is HIV Eradication
Possible, June 18, New York. Contact: Saint Vincents
Education & Training Department, Max Vaval or Andrew
Boreland, phone 212/228-8000 x243 or x231.
** Fourth International Symposium on Clinical Immunology,
June 19-22, Amsterdam, The Netherlands. Contact: Conference
Secretariat, Fourth International Symposium on Clinical
Immunology, Amsterdam RAI-OBA, P.O. Box 77777, 1070 MS
Amsterdam, The Netherlands. Web site
http://www.rai.nl/congress/cic/en/welcome.html.
July 1997
** FDA Antiviral Drugs Advisory Committee, July 14-15, also
July 16, Silver Spring, Maryland. Contact: FDA, 301/443-5455.
(See separate announcement in this issue.)
** AIDS Clinical Trial Group (ACTG), July 19-22, Washington,
D.C. Contact: NIAID, 301/496-8215.
August 1997
** HIV/AIDS in Cuba: Building Bridges, Crossing Borders,
August 6-13, Havana, Cuba. Contact: U.S.- Cuba Medical
Project, One Union Square West, Suite 211, New York, NY
10003. 212/727-3247, fax 212/727-3265, email
uscubamed@igc.apc.org.
** National Black Nurses Association, 25th Institute and
Annual Conference, August 7-10, New York, NY. Contact: NBNA,
1511 K Street NW, Suite 415, Washington, D.C. 20005; 202/393-
6870, fax 202/347-3808.
** The 15th Annual Symposium of the Gay & Lesbian Medical
Association, August 21-23, San Francisco, California.
Contact: GLMA Symposium, 459 Fulton St., Suite 107, San
Francisco, CA 94102; 415/255-4547, fax 415/255-4784, email
gaylesmed@aol.com, web site http://www.glma.org.
** Clinical Care of the AIDS Patient: Summer Symposium,
August 21-26, Sun Valley, Idaho. Contact: Department of
Medicine at the University of California San Francisco,
School of Medicine, 415/476-5208, web site
http://cme.ucsf.edu/.
September 1997
** A Conference on Global Strategies for the Prevention of
HIV Transmission From Mothers to Infants, September 3-6,
Washington, D.C.
Logistics and abstract submission: Contact Ms. Andrea Hall,
Social & Scientific Systems, Inc., 7101 Wisconsin Ave., Suite
1300, Bethesda, MD 20814-4805; 800/749-9620 (U.S. calls
only), 301/986-1216 (dedicated meeting phone number),
301/986-4870 (accepts collect calls from outside the United
States for "Global Strategies Conference" between 9:00 a.m.
and 5:00 p.m. Eastern time), fax 301/913-0351, email adh@s-
3.com. (Dates: Early registration by July 3 receives
discount. Abstracts due by June 27, late-breaking research by
August 15.)
Scientific Program: Contact Arthur Ammann, M.D., 415/451-
1814, fax 415/456-2622, email Ammanndoc@aol.com.
** Community Programs for Clinical Research on AIDS (CPCRA),
September 4-5, Washington, D.C. Contact: Elaine Allison,
CPCRA Operations Office, 301/230-9670, fax 301/230-7190,
email eallison@opsctr.s-3.com.
** AIDS, Medicine and Miracles: 10th Annual HIV Conference
Retreat, September 4-7, Phoenicia, New York. Contact: AIDS,
Medicine and Miracles, 800/875-8770, email amm@csd.net.
** HIV-1 Infection, Mucosal Immunity & Pathogenesis,
September 11-13, Natcher Conference Center, National
Institutes of Health, Washington, D.C. Contact: Mr. Fred
Hill, Conference Manager, HIV-1 Infection, Mucosal Immunity &
Pathogenesis, c/o ComputerCraft Corporation, 6707 Democracy
Blvd., Suite 101, Bethesda, MD 20817; 301/493-9674, fax
301/530-0634. (Registration Deadline: August 1, 1997; due to
space limitations, early registration is encouraged.)
** International Congress on Biomedical Peer Review and
Global Communications, September 17-21, Prague, Czech
Republic. Contact: Annette Flanagin, American Medical
Association, 515 N. State St., Chicago, IL 60610; 312/464-
2432, fax 312/464-5824.
** United States Conference on AIDS, September 18-21, Miami
Beach, FL., sponsored by the National Minority AIDS Council
(NMAC) Contact: Conference Registrar, The United States
Conference on AIDS, 1931 13th St. NW, Washington, D.C. 20009-
4432; 202/483-6622 x313, fax 202/483-1127.
** 37th Annual Meeting of the Interscience Conference on
Antimicrobial Agents and Chemotherapy (ICAAC), September 28-
October 1, Toronto, Ontario, Canada. Contact: American
Society for Microbiology (ASM), Meetings Department, 1325
Massachusetts Ave. NW, Washington, D.C. 20005-4171; 202/942-
9356, fax 202/942-9340. [Comment: ICAAC is likely to be
important this year, because in odd-numbered years there is
no International Conference on AIDS (now named World AIDS
Conference) to draw research presentations away. Note: Future
ICAAC meetings have been scheduled for September 1998 in San
Diego, and September 1999 in San Francisco.]
October 1997
** 6th European Conference on Clinical Aspects and Treatment
of HIV Infection, October 11-15, Hamburg, Germany. Contact:
K.I.T. GmbH, Kingress und Incentive-Organisation, Karl-
Liebknecht Strasse 5, D-10178 Berlin, Germany; +49 30 2382
6900, fax +49 30 2382 6940, email hiv@kit.de, web site
http://www.kit.de.
** Sixth Regional Symposium on the Design & Methods of
Clinical Trials, October 17-18, San Francisco. Contact:
Office of Continuing Medical Education, University of
California, San Francisco, 415/476-5808 to register, 415/476-
4251 to receive a brochure when it is available.
** International Congress of Sexually Transmitted Diseases,
October 19-22, Seville, Spain. Contact: International
Congress of STD, Apartado 6077, 41080 Seville Spain; +34 5
4903409, fax +34 5 4377413. Or, HCC/ICSTD, One Bridge Plaza,
Suite 350, Fort Lee, NJ, 07024, 201/947-5545, fax 201/947-
8406.
** 3rd Annual Conference: A Time for Healing--Women and HIV,
October 22-24, Las Vegas, NV. Contact: Pat Stachewicz or
Marlo Tonge, 702/383-1397.
** 4th International Congress on AIDS in Asia and the
Pacific, October 25-29, Manila, Philippines. Contact:
Secretariat, 2nd Floor, Physicians' Tower, 533 United Nations
Ave., Ermita, Manila 1000, Philippines; +63 2 526-8103, or
+63 2 526-8105, fax +63 2 522-1090 or +63 2 522-8130, email
aidsphil@philonline.com.ph, web site
http://www.hain.org/aidsphil.html.
November 1997
** GNP 8th International Conference for People Living with
HIV/AIDS, November 5-12, Chiang Mai, Thailand. Contact:
GNP/ICW Conference Secretariat, 12/14 Rajchiangsaen Road,
Soi 2 Kot, Haiye, Chiang Mai 50100, Thailand, phone 53 206 760,
fax 53 206 761, email gnpicw8@loxinfo.co.th;
Or, Conference Secretariat, Bangkok, +66 2 526 8311, fax +66 2
968 8021, email capisuk@mozart.inet.co.th. Or, GNP+ central
Secretariat, Amsterdam, +31 20 689 8218, fax +31 20 689 8059,
email gnp@gn.apc.org. Or, ICW Secretariat, London, +44 171
222 1333, fax +44 171 222 1242, email icw@gn.apc.org.
TEL: 53 206 760
FAX: 53 206 761
EMAIL: gnpicw8@loxinfo.co.th
** Tenth Annual Association of Nurses in AIDS Care
Conference, November 6-9, Miami Beach, FL. Contact: ANAC
Tenth Annual Conference, 11250 Roger Bacon Dr., Suite 8,
Reston, VA 20190-5202; 800/260-6780.
** National AIDS Treatment Advocates Forum, November 9-12,
San Diego, CA. Contact: David Barre, NATAF Registration, c/o
National Minority AIDS Council, 1931 13th Street NW,
Washington, D.C. 20009; 202/483-6622 x327, fax 202/483-1135,
email NMACtx@aol.com
** Healthcare Resource Allocation for HIV/AIDS and Other
Life-Threatening Illnesses, November 10-11, Washington, D.C.
Contact: Paul Rathe, International Association of Physicians
in AIDS Care, 312/419-7074, fax 312/419-7079, email
conference@iapac.org.
** International Conference on AIDS Wasting, (title may
change), November 16-19, Ft. Lauderdale, Florida. Contact:
IFARA (International Foundation for Alternative Research on
AIDS), 954/630-8002.
December 1997
** Clinical Care of the AIDS Patient, December 4-6, Palace
Hotel, San Francisco. Contact: University of California San
Francisco, Department of Medicine, Postgraduate Programs, Box
0656, San Francisco, CA 94143-0656; phone 415/476-5208, web
site http://cme.ucsf.edu/.
** AIDS Clinical Trial Group (ACTG), December 5-10,
Washington, D.C. Contact: NIAID, 301/496-8215.
** Xth International Conference on AIDS & STD in Africa,
December 7-11, Abidjan, Cote d'Ivoire. Contact: Programme
National de Lutte contre le SIDA les MST et al Tuberculose,
04 BP 2113, Abidjan 04, Cote d'Ivoire; +225 243013, or +225
243014, or +225 244306, fax +225 243119, web
http://www.us.unaids.org/lowband/events/abidjan/introduction.
html
1988
** T Lymphocyte Activation, Differentiation and Death,
January 26-February 1, Keystone, Colorado. Contact: Keystone
Symposia, Drawer 1630, Silverthorne, CO 80498; 800/253-0685
or 970/262-1230, fax 970/262-1525, email
keystone@symposia.com, web site
http://www.colorado.net/symposia.
** 5th Conference on Retroviruses and Opportunistic
Infections, late January or early February, 1998. In previous
years this conference has been held in Washington D.C., but
other cities are now being considered.
** Molecular Aspects of Viral Immunity, February 16-22,
Tamarron, Colorado. Contact: Keystone Symposia, Drawer 1630,
Silverthorne, CO 80498; 800/253-0685 or 970/262-1230, fax
970/262-1525, email keystone@symposia.com, web site
http://www.colorado.net/symposia.
** Cell and Molecular Biology of Dendritic Cells, March 7-13,
Santa Fe, New Mexico. Contact: Keystone Symposia, Drawer
1630, Silverthorne, CO 80498; 800/253-0685 or 970/262-1230,
fax 970/262-1525, email keystone@symposia.com, web site
http://www.colorado.net/symposia.
** HIV Pathogenesis and Treatment, March 13-19, Park City,
Utah. Contact: Keystone Symposia, Drawer 1630, Silverthorne,
CO 80498; 800/253-0685 or 970/262-1230, fax 970/262-1525,
email keystone@symposia.com, web site
http://www.colorado.net/symposia.
** Angiogenesis and Vascular Remodelling, March 28-April 3,
Steamboat Springs, Colorado. Contact: Keystone Symposia,
Drawer 1630, Silverthorne, CO 80498; 800/253-0685 or 970/262-
1230, fax 970/262-1525, email keystone@symposia.com, web site
http://www.colorado.net/symposia.
** TB: Molecular Mechanisms and Immunologic Aspects, April 2-
8, Keystone, Colorado. Contact: Keystone Symposia, Drawer
1630, Silverthorne, CO 80498; 800/253-0685 or 970/262-1230,
fax 970/262-1525, email keystone@symposia.com, web site
http://www.colorado.net/symposia. (Note: registration for
this conference also allows for attendance at the meeting
below.)
** Opportunistic Infections in AIDS, April 2-8, Keystone,
Colorado. Contact: Keystone Symposia, Drawer 1630,
Silverthorne, CO 80498; 800/253-0685 or 970/262-1230, fax
970/262-1525, email keystone@symposia.com, web site
http://www.colorado.net/symposia. (Note: registration for
this conference also allows for attendance at the meeting
above.)
** 12th World AIDS Conference, June 28 - July 3, 1998,
Geneva. Deadline for regular abstract submission, and for
scholarship applications, is February 2, 1988. Contact:
Secretariat, 94 rue des Eaux-Vives, CH-1207 Geneva,
Switzerland; phone +41 22 737 33 44, fax +41 22 700 33 11,
email info@aids98.ch, web site http://www.aids98.ch.
** 4th International Congress on Drug Therapy in HIV
Infection, November 8-12, 1998, Glasgow, Scotland. Contact:
Gardiner- Caldwell Communications Ltd., +44-1625-664000, fax
+44-1625-610260.
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